Depositional (platelet) thrombus I82.9

Thrombosis in general is the process of intravital, intravascular blood clotting (Nennstiel 2019). A deposition thrombus represents the classic form of thrombosis in the arteries (Kasper 2015) or the ventricles and atria (Claus 2019).

It rarely occurs in isolation (Schindler 2021).

Thrombi are differentiated between a:

- Clotting thrombus, the so-called red thrombus with a smooth surface (Herold 2022), also known as "tail thrombus".

- septal thrombus, the so-called white thrombus

- mixed thrombus

This consists of a head part, the deposition thrombus, and a tail part, the coagulation th rombus (Schindler 2021).

Arterial thrombi are a major cause of morbidity and mortality in a variety of arterial diseases. They are responsible for approximately 33% of all deaths (Kasper 2015).

The incidence of critical arterial occlusions in Europe and North America is estimated to be approximately 500-1,000 per 1 million population per year (Ludwig 2020).

Peripheral arterial occlusions affect the lower extremity in up to 85% (Töpfer 2023).

The causes of thrombus formation are summarized in the Virchow triad:

- I. Disruption or alteration of the vessel wall.

These can be caused by e.g.

- trauma

- arteriosclerosis

- great mechanical stress

- ischemia

All of the above factors can lead to damage to the endothelium, resulting in a lack of antithrombogenic substances and thus thrombin formation (Nennstiel 2019).

- II. disturbance of hemodynamics

Disorders of hemodynamics include a:

- Slowing of blood flow due to, e.g.

- Compression of the vessels

- Enlargement of the vessels (e.g., in varices)

- increase of hematocrit

- Increase of the viscosity of the blood

- Obstruction of the lumen

- Vortex formation, especially at passage obstacles, vessel branches and aneurysms

- Acceleration of blood flow due to, for example, hypertension, in which platelets are pressed against the vessel wall (Nennstiel 2019)

- III. disturbance of the blood composition

Blood composition disorder may occur due to:

- Increase in platelet count due to, e.g.

- Neoplasia of the hematopoietic system. This may lead to increased platelet activation.

- Increase in cell count due to e.g.

- Decrease in serum. Increased blood viscosity may lead to slowing of flow.

- Neoplasms

- Paraneoplastic syndrome in e.g.

- metastatic carcinoma. In this case, the carcinoma itself produces increased procoagulant substances.

- Hereditary disorders, e.g.

- Factor V Leiden mutation

- Postoperative or after injuries

- In this case, there are more clotting factors than normal in the blood due to tissue damage (Nennstiel 2019).

- Medication due to e.g. anticonceptives

- During pregnancy (Nennstiel 2019).

A deposition thrombus forms when blood flow is maintained and is caused by, for example, an atherosclerotically altered arterial wall, in inflamed vessels (e.g., in arteritis, thrombophlebitis), aneurysms, in mitral valve defects in the left atrium, in myocardial infarctions, etc. (Weimann 2002).

The risk of formation of a deposition thrombus in the form of myocardial infarction or apoplexy is significantly increased during bacterial or viral infections. Secretion thrombi also contribute to the high mortality in the context of sepsis (Kasper 2015).

Initially, a defect of the endothelium occurs (Herold 2022). This exposes subendothelial components that are responsible for the subsequent platelet activity (Kasper 2022), also referred to as "viscous metamorphosis" (Nennstiel 2019).

Platelets now attach to the site of the endothelial defect by adhesion and aggregation. The thrombus that forms does not fill the entire lumen of the vessel, but adheres firmly to the vessel wall (Herold 2022). Platelet adhesion activates thrombin (Kasper 2015), which plays an important role in the formation of a deposition thrombus by promoting platelet aggregation and fibrin formation (Nennstiel 2019).

In the case of a deposition thrombus in the extremities, there are:

- acute pain

- Pulselessness in the affected extremity

- pallor of the affected extremity (Schölmerich 2003)

The cardinal symptoms of a peripheral arterial occlusion are also summarized by the so-called "6 Ps":

- Pain

- Paleness (pallor)

- Pulselessness

- Paresthesia (sensory disturbances)

- Paralysis (inability to move)

- Prostration (symptoms of shock)

(Potter 2023)

Symptoms of myocardial infarction s. d.

In case of suspicion of a deposition thrombus, imaging diagnostics should be performed immediately in the form of color duplex or compression sonography, angiography or ascending phlebography (Schölmerich 2003).

Ascending phlebography

This examination is the method of choice for detecting thrombosis (Ludwig 2020).

Sonographically, a deposition thrombus can be visualized in an echo-poor stratified and banded fashion (Schmidt 2002).

Angio- CT

This shows in particular the stenosis of the affected vessel caused by the deposition thrombus (Eichler 2016).

Determination of D- dimers

This allows the disease activity of an artherosclerotic disease to be assessed, as increased D- dimers indicate increased fibrin turnover (Pötzsch 2002).

A white thrombus is found, which is poor in erythrocytes and has a corrugated surface (Herold 2022). The thrombus shows periodic layering of platelets and networks of fibrin, with embedded erythrocytes and leukocytes, oriented perpendicular to the direction of blood flow. This gives the thrombus a coral stick-like appearance (Nüllen 2014).

Histiocytes are found at the boundary between the thrombus and the intima. The platelets are no longer recognizable as individual platelets; rather, a homogeneous mass is found due to aggregation (Nüllen 2014).

- Organ occlusions

- Organ infarctions (Claus 2019)

- Vascular occlusion with loss of an extremity (Claus 2019)

The primary therapeutic goal is to remove the occluding thrombus. For this purpose, it is important not to exceed the ischemia tolerance, because thereafter even reopening of the vessel cannot prevent permanent tissue damage (Pötzsch 2002).

Septal thrombi of the extremities, for example, must be recanalized within 6 h, otherwise there is a risk of irreversible ischemia with loss of the affected extremity (Schölmerich 2003).

The only exception is the reopening of chronically occluded coronary vessels (Pötzsch 2002).

Various options are available for reopening the affected vessel:

- thrombectomy

- catheter-based recanalization

- stent implantation

- fibrinolytic therapy (Pötzsch 2002)

This involves substances that stimulate the body's own fibrinolysis. These include urokinase, streptokinase and alteplase (Hallbach 2021). For more information, see Fibrinolytics.

Drug treatment of sequestration thrombi can be achieved by platelet aggregation inhibitors of the GPII b / III a receptor antagonist groups (Buchta 2004). These block the GP- II b / III a receptor on the platelet surface, which is important for aggregation (Huch 2019).

Preparations in these groups include, for example, abciximab (trade name RheoPro), eptifibatide (trade name Integrilin) and tirofiban (trade name Aggrastat).

(Buchta 2004).

Arterial thrombi can be prevented prophylactically by administration of platelet aggregation inhibitors such as ASA (Claus 2019), because ASA inhibits platelet aggregation by inhibiting thromboxane A2 formation (Huch 2019). Dosage recommendation: ASA 100 mg / d. If contraindications to ASA exist, clopidogrel at the dosage of 75 mg / d can be used alternatively (Pötzsch 2002).

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